Dendrodendritic recurrent excitation in mitral cells of the rat olfactory bulb

Most neuronal interactions within the olfactory bulb network are mediated b y dendrodendritic synapses. Dendritic transmitter release potentially could affect the parent dendrite as well as local neuronal elements that have re ceptors for the released transmitter. Here we report that under conditions that facilitate N-methyl-D-aspartate (NMDA) receptor activity (reduced GABA (A) inhibition and extracellular Mg2+), a single action potential evoked by brief intracellular current pulses in mitral cells is followed by a prolon ged depolarization, which is blocked by an NMDA receptor antagonist. This d epolarization also is evoked by a presumed calcium spike in the presence of tetrodotoxin. A similar NMDA-receptor-dependent prolonged depolarization i s elicited by stimulation of the lateral olfactory tract at current intensi ties subthreshold for antidromic activation of the recorded neuron. These o bservations suggest that glutamate released from the dendrites of mitral ce lls excites the same and neighboring mitral cell dendrites. Further evidenc e suggests that both the apical and lateral dendrites of mitral cells parti cipate in this recurrent excitation. These dendrodendritic interactions may play a role in the prolonged, NMDA-receptor-dependent depolarization of mi tral/tufted cells evoked by olfactory nerve stimulation.